A 65-year-old female presented with fatigue, constipation, feeling cold, dry skin, and neck swelling. On examination, she had an enlarged, nontender thyroid, diminished reflexes, dry skin, and was taking fortified salt.
The most likely diagnosis is hypothyroidism. Laboratory tests would include measuring thyroid stimulating hormone (TSH) levels to confirm the diagnosis. Treatment would be thyroid hormone replacement therapy.
its all about thyroid gland,functions of thyroid gland,disorders of thyroid gland,signs and symptoms and medications.hope it will be useful for you.thank you,
The document discusses a case of subclinical hypothyroidism in a 70-year-old woman named Ayesha who presented with fatigue, dry skin, and difficulty losing weight. Laboratory tests found her TSH level to be elevated at 8.1 mIU/L and her FT4 level to be low normal, confirming a diagnosis of subclinical hypothyroidism likely caused by Hashimoto's thyroiditis. The document then provides information on hypothyroidism, its causes, signs and symptoms, diagnosis, and treatment options including levothyroxine replacement therapy.
The document provides information about thyroid gland disorders including hypothyroidism and hyperthyroidism. It discusses the anatomy and blood supply of the thyroid gland. It describes Hashimoto's thyroiditis as the most common cause of hypothyroidism due to an autoimmune reaction. Graves' disease is outlined as the most common cause of hyperthyroidism, also caused by an autoimmune process involving thyroid stimulating antibodies. The clinical features, investigations, and treatment approaches for hypothyroidism and hyperthyroidism are summarized.
This document discusses the synthesis of thyroid hormones by the thyroid gland. It describes how thyroid stimulating hormone regulates the thyroid and stimulates iodine uptake. The thyroid then synthesizes thyroxine (T4) and triiodothyronine (T3) by oxidizing and binding iodine to thyroglobulin. T4 makes up most of the secreted hormones and is later converted to the active T3 hormone in other tissues. The hormones are transported bound to carrier proteins and only the free fractions have metabolic effects.
Hyperthyroidism can be diagnosed based on clinical presentation and lab tests showing suppressed TSH and elevated FT4 and FT3. It is classified as Graves' disease, toxic multinodular goiter, or toxic adenoma based on thyroid antibodies and nuclear scintigraphy. Treatment options include anti-thyroid medications, radioactive iodine therapy, and surgery. Anti-thyroid drugs are first line treatment for Graves' disease, while radioactive iodine or surgery is recommended for toxic nodular conditions. Surgical treatment is reserved for cases where other options are contraindicated or not effective.
This document discusses a case of hyperthyroidism in a 39-year-old female presenting with nervousness, anxiety, palpitations, diarrhea, and weight loss. On examination, she had a heart rate of 110 bpm, tremor, increased reflexes, and an enlarged thyroid. Laboratory tests found high free T3 and T4, low TSH, and positive thyroid stimulating immunoglobulins, consistent with a diagnosis of Graves' disease. Graves' disease is an autoimmune disorder causing hyperthyroidism through thyroid stimulating antibodies. If left untreated, hyperthyroidism can progress to a thyroid storm, a life-threatening condition of severe hypermetabolism.
The document summarizes the thyroid gland and its hormone production. It discusses:
- The thyroid gland's location in the neck and its lobes/isthmus.
- The three hormones it produces: thyroxine, triiodothyronine, and calcitonin.
- The process of hormone biosynthesis, including iodine trapping, oxidation, thyroglobulin synthesis, iodination of tyrosine, and coupling reactions to form T3 and T4.
- Storage of hormones in thyroglobulin vesicles and their release into blood circulation.
The thyroid gland secretes three hormones: T3, T4, and calcitonin. T3 and T4 regulate metabolism, while calcitonin regulates calcium levels. The thyroid is located in the neck below the Adam's apple. T3 and T4 are synthesized from tyrosine and stored bound to thyroglobulin. They are regulated by TSH from the pituitary and feedback to decrease TSH secretion. The main actions of thyroid hormones are to increase growth, metabolism, and heart rate. Hypothyroidism is treated with thyroxine replacement therapy.
its all about thyroid gland,functions of thyroid gland,disorders of thyroid gland,signs and symptoms and medications.hope it will be useful for you.thank you,
The document discusses a case of subclinical hypothyroidism in a 70-year-old woman named Ayesha who presented with fatigue, dry skin, and difficulty losing weight. Laboratory tests found her TSH level to be elevated at 8.1 mIU/L and her FT4 level to be low normal, confirming a diagnosis of subclinical hypothyroidism likely caused by Hashimoto's thyroiditis. The document then provides information on hypothyroidism, its causes, signs and symptoms, diagnosis, and treatment options including levothyroxine replacement therapy.
The document provides information about thyroid gland disorders including hypothyroidism and hyperthyroidism. It discusses the anatomy and blood supply of the thyroid gland. It describes Hashimoto's thyroiditis as the most common cause of hypothyroidism due to an autoimmune reaction. Graves' disease is outlined as the most common cause of hyperthyroidism, also caused by an autoimmune process involving thyroid stimulating antibodies. The clinical features, investigations, and treatment approaches for hypothyroidism and hyperthyroidism are summarized.
This document discusses the synthesis of thyroid hormones by the thyroid gland. It describes how thyroid stimulating hormone regulates the thyroid and stimulates iodine uptake. The thyroid then synthesizes thyroxine (T4) and triiodothyronine (T3) by oxidizing and binding iodine to thyroglobulin. T4 makes up most of the secreted hormones and is later converted to the active T3 hormone in other tissues. The hormones are transported bound to carrier proteins and only the free fractions have metabolic effects.
Hyperthyroidism can be diagnosed based on clinical presentation and lab tests showing suppressed TSH and elevated FT4 and FT3. It is classified as Graves' disease, toxic multinodular goiter, or toxic adenoma based on thyroid antibodies and nuclear scintigraphy. Treatment options include anti-thyroid medications, radioactive iodine therapy, and surgery. Anti-thyroid drugs are first line treatment for Graves' disease, while radioactive iodine or surgery is recommended for toxic nodular conditions. Surgical treatment is reserved for cases where other options are contraindicated or not effective.
This document discusses a case of hyperthyroidism in a 39-year-old female presenting with nervousness, anxiety, palpitations, diarrhea, and weight loss. On examination, she had a heart rate of 110 bpm, tremor, increased reflexes, and an enlarged thyroid. Laboratory tests found high free T3 and T4, low TSH, and positive thyroid stimulating immunoglobulins, consistent with a diagnosis of Graves' disease. Graves' disease is an autoimmune disorder causing hyperthyroidism through thyroid stimulating antibodies. If left untreated, hyperthyroidism can progress to a thyroid storm, a life-threatening condition of severe hypermetabolism.
The document summarizes the thyroid gland and its hormone production. It discusses:
- The thyroid gland's location in the neck and its lobes/isthmus.
- The three hormones it produces: thyroxine, triiodothyronine, and calcitonin.
- The process of hormone biosynthesis, including iodine trapping, oxidation, thyroglobulin synthesis, iodination of tyrosine, and coupling reactions to form T3 and T4.
- Storage of hormones in thyroglobulin vesicles and their release into blood circulation.
The thyroid gland secretes three hormones: T3, T4, and calcitonin. T3 and T4 regulate metabolism, while calcitonin regulates calcium levels. The thyroid is located in the neck below the Adam's apple. T3 and T4 are synthesized from tyrosine and stored bound to thyroglobulin. They are regulated by TSH from the pituitary and feedback to decrease TSH secretion. The main actions of thyroid hormones are to increase growth, metabolism, and heart rate. Hypothyroidism is treated with thyroxine replacement therapy.
The document discusses the thyroid gland and hypothyroidism. It provides details on the anatomy, histology, synthesis and secretion of thyroid hormones. It also describes the clinical features of hypothyroidism including constitutional symptoms like cold intolerance and fatigue. Laboratory tests for investigating thyroid function and disorders are outlined, including measurement of thyroid hormones and thyroid antibodies. Physical examination findings for the thyroid gland are also reviewed.
The document discusses the thyroid gland and thyroid disorders. It provides details on:
- The anatomy and blood supply of the thyroid gland.
- Thyroid follicles which are the functional units that secrete thyroid hormones like T4 and T3.
- The two main thyroid disorders - hypothyroidism which is an underactive thyroid, and hyperthyroidism which is an overactive thyroid.
- The most common causes of hypothyroidism including Hashimoto's thyroiditis, and the signs, symptoms, and treatment which involves thyroid hormone replacement.
- Graves' disease as the most common cause of hyperthyroidism, along with its autoimmune pathogenesis and associated signs and
Thyroid function test ( TFT) in simple waybinaya tamang
This document provides information about thyroid function tests. It discusses the thyroid gland, thyroid hormones, and thyroid stimulating hormone. It covers the biological functions of thyroid hormones, their biochemistry and biosynthesis. It also describes hypothyroidism and hyperthyroidism, their causes, classifications, and clinical presentations. The role of thyroid stimulating hormone is explained. Additionally, the document outlines objectives of thyroid function tests and different classifications of tests based on their function.
Thyroid Gland and Disease of Thyroid GlandRanadhi Das
The thyroid gland is one of the largest endocrine glands.
The thyroid gland is located immediately below the larynx and anterior to the upper part of the trachea. It weighs about 15-20g.
It consists of 2 lateral lobes connected by a narrow band of thyroid tissue called the isthmus.
The isthmus usually overlies the region from the 2nd to 4th tracheal cartilage.
The document discusses the thyroid gland and thyroid disorders. It begins by describing the anatomy and function of the thyroid gland, which produces thyroid hormones that regulate metabolism. It then discusses various thyroid disorders including hyperthyroidism (overproduction of hormones), such as Graves' disease, and hypothyroidism (underproduction of hormones), such as Hashimoto's thyroiditis. The document outlines the symptoms, signs, causes and treatments of both hyperthyroidism and hypothyroidism and their effects on the body. It also describes the hypothalamic-pituitary-thyroid feedback system that regulates thyroid hormone levels.
The document discusses thyroid disorders and summarizes key information about the thyroid gland, its hormones and functions. It describes hypothyroidism and hyperthyroidism, their causes, symptoms and treatment methods. Hypothyroidism is treated mainly with levothyroxine while hyperthyroidism can be treated with antithyroid drugs, beta blockers or radioactive iodine ablation.
a brief on thyroid gland covering following titles:
Introduction
Anatomy and physiology of thyroid gland
Synthesis of thyroid hormones
Regulation
Mechanism of action
Biological function
The thyroid is a small, butterfly-shaped gland located at the base of your neck just below the Adam’s apple.
Several different disorders can arise when your thyroid produces too much hormone (hyperthyroidism) or not enough (hypothyroidism).
Four common disorders of the thyroid are Hashimoto’s disease, Graves’ disease, goiter, and thyroid nodules.
AUM ENT Clinic is dedicated to the delivery of compassionate, quality, state-of-the-art and cost effective health care with best-in-class technology and equipment.
Contact us @https://www.aumentclinic.com/contact-us.php
The document summarizes thyroid hormone synthesis and regulation. Iodine is incorporated into thyroglobulin to form the thyroid hormones thyroxine (T4) and triiodothyronine (T3). T4 is formed by coupling of two diiodotyrosine molecules, while T3 results from coupling a diiodotyrosine and a monoiodotyrosine. Only a small fraction of T4 and T3 circulate freely in the blood; the majority are bound to proteins. The free forms, free T4 and free T3, are biologically active. Thyroid stimulating hormone (TSH) regulates thyroid hormone production through negative feedback. Laboratory tests of TSH, total T4, total T3,
The document discusses thyroid hormones and thyroid function tests. It states:
- The thyroid gland produces thyroxine (T4) and triiodothyronine (T3), which regulate metabolic rate. Iodine is essential for their synthesis.
- TSH secretion is regulated by a negative feedback loop involving the hypothalamus and pituitary gland. Thyroid hormones inhibit TSH release.
- Thyroid function tests measure thyroid hormones, binding proteins, antibodies, and other markers. Direct and indirect methods estimate free thyroid hormones.
- Abnormal test results can indicate primary or secondary hypothyroidism/hyperthyroidism, autoimmune disease, or other conditions. Serial testing
The document discusses thyroid disorders and provides information about:
1) The thyroid gland, its location and functions including producing thyroid hormones that regulate metabolism.
2) Types of thyroid disorders like hypothyroidism and hyperthyroidism, their causes, symptoms and treatment options.
3) Diagnostic tests for thyroid disorders including thyroid function tests and scans.
4) Specific conditions like Graves' disease, Hashimoto's thyroiditis, thyroid storm and their characteristics.
This document discusses thyroid hormones, their functions, synthesis, regulation, and mechanisms of action. It covers the receptors, transporters, and enzymes involved in thyroid hormone activity. It also describes the clinical features and management of hypothyroidism and hyperthyroidism, as well as laboratory tests for thyroid function. Various thyroid analogs and their selective actions on thyroid hormone receptors are also mentioned.
This presentation about thyroid gland :
- Anatomy of thyroid gland
- Physiology of thyroid gland
- Pathology of thyroid gland
- Treatment and prevention of thyroid disease
The thyroid gland produces three main hormones: T4, T3, and calcitonin. T4 is produced in larger amounts than T3. Both are produced through a process involving iodine uptake and binding to tyrosine residues on thyroglobulin within the thyroid follicle. T3 has greater biological activity than T4. Hypothyroidism occurs when not enough hormones are produced, while hyperthyroidism is an overproduction. Diseases are treated through antithyroid drugs, radioactive iodine therapy, or thyroid surgery.
The thyroid gland regulates metabolism and plays a key role in many body functions. Hypothyroidism occurs when the thyroid gland is underactive and does not produce enough hormones. It can be caused by autoimmune diseases like Hashimoto's thyroiditis or problems with the pituitary gland. Symptoms include fatigue, weight gain, dry skin and hair, and feeling cold. Blood tests are used to diagnose hypothyroidism by measuring thyroid stimulating hormone and thyroid hormone levels. Lifelong thyroid hormone replacement therapy is needed to treat hypothyroidism and prevent serious complications like myxedema coma.
The thyroid gland secretes two major hormones: thyroxine (T4) and triiodothyronine (T3). These hormones increase the metabolic rate of the body and are controlled by thyroid-stimulating hormone (TSH) from the pituitary gland. The thyroid traps iodine from the blood and uses it to synthesize T4 and T3 within thyroglobulin follicles. Most secreted hormone is T4, which is later converted to the more potent T3 in tissues. Thyroid hormones increase metabolism, growth, and heart rate by activating nuclear transcription of genes in cells throughout the body. TSH secretion from the pituitary is regulated by thyrotropin-releasing hormone from the hyp
This document discusses thyrotoxicosis, which results from excess thyroid hormone production regardless of cause. It is one of the more common endocrine disorders seen by family physicians. The causes of thyrotoxicosis include Graves' disease, toxic multinodular goiter, solitary toxic nodule, and thyroiditis. Graves' disease is an autoimmune condition characterized by a diffuse goiter, ophthalmopathy, and dermopathy. Toxic multinodular goiter develops from autonomy in a pre-existing nodular goiter. A solitary toxic nodule refers to autonomy developing in an otherwise normal thyroid. Thyroiditis can cause a transient thyrotoxic phase followed by hypothyroidism. Treatment depends on
Thyroid Function Tests, NORMAL THYROID PHYSIOLOGY
, Anatomy of the Thyroid Gland, Hypothalamic-Pituitary-Thyroid AxisNegative Feedback Mechanism, Hypothalamic-Pituitary-Thyroid AxisPhysiology, PITUITARY-THYROTROPE CELL
, THYROID HORMONES
, FORMATION & SECRETION OF THYROID HORMONES , ION TRANSPORT BY THE THYROID FOLLICULAR CELL
, THYROGLOBULIN SYNTHESIS IN THE THYROID FOLLICULAR CELL
Thyroid and its pathology (Hypothyroidism).Vikas Reddy
GREEK :- THYREOS – SHIELD ; EIDOS – FORM
1.LOCATION:- Anterior to trachea in between the cricoid cartilage and the suprasternal notch.
2.SHAPE:- It has 2 lobes connected with an isthmus, each lobe in turn has two poles.
3.Weighs around 10-20 gm, highly vascular and soft in consistency.
4. 4 Parathyroid glands which secrete PTH are located posterior to each pole of thyroid
The RLN traverse the lateral border of thyroid gland and must be identified during thyroid surgery to avoid injury and vocal cord paralysis.
Develops from the floor of primitive pharynx during the 3rd week of gestation.
Fetal cells in which developmental transcription factors TTF-1,TTF-2 & PAX-8 are expressed selectively form the thyroid gland ,secondly they result in induction of thyroid specific genes
Tg,TPO,NIS,TSH-R.
Mutations-THYROID AGENESIS & DYSHORMONOGENESIS(CONG. HYPOTHYROIDISM).
The developing gland migrates along the thyroglossal duct to reach its final location in the neck.
LINGUAL THYROID AND THYROGLOSSAL DUCT CYST.
Thyroid hormone synthesis begins at about 11 weeks of gestation.
Until 11 week of gestation and even later, it is the maternal thyroid hormones which cross the placenta to reach the fetus and aid its development.
Therefore a child born to a hypothyroid mother would suffer from features of congenital hypothyroidism.
Secondly if the mother has TSH-R blocking antibodies or has received anti thyroid therapy during pregnancy, might lead to transient congenital hypothyroidism.
The thyroid gland secretes three main hormones: T4, T3, and calcitonin. T4 is secreted in larger amounts than T3 but T3 has higher biological activity. The thyroid takes up iodine from the bloodstream which is then oxidized and used to iodinate tyrosine residues on thyroglobulin in the follicles. Coupling of iodinated tyrosines produces T4 and T3 which are stored in the follicles bound to thyroglobulin. TSH stimulates release of T4 and T3 into the bloodstream where most is bound to proteins while a small amount is free and biologically active. T4 can be converted to the more active T3 in other tissues
Thyroid function tests (TFTs) are the most frequently ordered endocrine investigations in children and adolescents.
Abnormalities in TFTs can help in diagnosis of primary thyroid disorders (i.e. disorders in which the defect is at the thyroid level) as well as secondary or central thyroid disorders (in which defect is at the pituitary level).
The document discusses the thyroid gland and hypothyroidism. It provides details on the anatomy, histology, synthesis and secretion of thyroid hormones. It also describes the clinical features of hypothyroidism including constitutional symptoms like cold intolerance and fatigue. Laboratory tests for investigating thyroid function and disorders are outlined, including measurement of thyroid hormones and thyroid antibodies. Physical examination findings for the thyroid gland are also reviewed.
The document discusses the thyroid gland and thyroid disorders. It provides details on:
- The anatomy and blood supply of the thyroid gland.
- Thyroid follicles which are the functional units that secrete thyroid hormones like T4 and T3.
- The two main thyroid disorders - hypothyroidism which is an underactive thyroid, and hyperthyroidism which is an overactive thyroid.
- The most common causes of hypothyroidism including Hashimoto's thyroiditis, and the signs, symptoms, and treatment which involves thyroid hormone replacement.
- Graves' disease as the most common cause of hyperthyroidism, along with its autoimmune pathogenesis and associated signs and
Thyroid function test ( TFT) in simple waybinaya tamang
This document provides information about thyroid function tests. It discusses the thyroid gland, thyroid hormones, and thyroid stimulating hormone. It covers the biological functions of thyroid hormones, their biochemistry and biosynthesis. It also describes hypothyroidism and hyperthyroidism, their causes, classifications, and clinical presentations. The role of thyroid stimulating hormone is explained. Additionally, the document outlines objectives of thyroid function tests and different classifications of tests based on their function.
Thyroid Gland and Disease of Thyroid GlandRanadhi Das
The thyroid gland is one of the largest endocrine glands.
The thyroid gland is located immediately below the larynx and anterior to the upper part of the trachea. It weighs about 15-20g.
It consists of 2 lateral lobes connected by a narrow band of thyroid tissue called the isthmus.
The isthmus usually overlies the region from the 2nd to 4th tracheal cartilage.
The document discusses the thyroid gland and thyroid disorders. It begins by describing the anatomy and function of the thyroid gland, which produces thyroid hormones that regulate metabolism. It then discusses various thyroid disorders including hyperthyroidism (overproduction of hormones), such as Graves' disease, and hypothyroidism (underproduction of hormones), such as Hashimoto's thyroiditis. The document outlines the symptoms, signs, causes and treatments of both hyperthyroidism and hypothyroidism and their effects on the body. It also describes the hypothalamic-pituitary-thyroid feedback system that regulates thyroid hormone levels.
The document discusses thyroid disorders and summarizes key information about the thyroid gland, its hormones and functions. It describes hypothyroidism and hyperthyroidism, their causes, symptoms and treatment methods. Hypothyroidism is treated mainly with levothyroxine while hyperthyroidism can be treated with antithyroid drugs, beta blockers or radioactive iodine ablation.
a brief on thyroid gland covering following titles:
Introduction
Anatomy and physiology of thyroid gland
Synthesis of thyroid hormones
Regulation
Mechanism of action
Biological function
The thyroid is a small, butterfly-shaped gland located at the base of your neck just below the Adam’s apple.
Several different disorders can arise when your thyroid produces too much hormone (hyperthyroidism) or not enough (hypothyroidism).
Four common disorders of the thyroid are Hashimoto’s disease, Graves’ disease, goiter, and thyroid nodules.
AUM ENT Clinic is dedicated to the delivery of compassionate, quality, state-of-the-art and cost effective health care with best-in-class technology and equipment.
Contact us @https://www.aumentclinic.com/contact-us.php
The document summarizes thyroid hormone synthesis and regulation. Iodine is incorporated into thyroglobulin to form the thyroid hormones thyroxine (T4) and triiodothyronine (T3). T4 is formed by coupling of two diiodotyrosine molecules, while T3 results from coupling a diiodotyrosine and a monoiodotyrosine. Only a small fraction of T4 and T3 circulate freely in the blood; the majority are bound to proteins. The free forms, free T4 and free T3, are biologically active. Thyroid stimulating hormone (TSH) regulates thyroid hormone production through negative feedback. Laboratory tests of TSH, total T4, total T3,
The document discusses thyroid hormones and thyroid function tests. It states:
- The thyroid gland produces thyroxine (T4) and triiodothyronine (T3), which regulate metabolic rate. Iodine is essential for their synthesis.
- TSH secretion is regulated by a negative feedback loop involving the hypothalamus and pituitary gland. Thyroid hormones inhibit TSH release.
- Thyroid function tests measure thyroid hormones, binding proteins, antibodies, and other markers. Direct and indirect methods estimate free thyroid hormones.
- Abnormal test results can indicate primary or secondary hypothyroidism/hyperthyroidism, autoimmune disease, or other conditions. Serial testing
The document discusses thyroid disorders and provides information about:
1) The thyroid gland, its location and functions including producing thyroid hormones that regulate metabolism.
2) Types of thyroid disorders like hypothyroidism and hyperthyroidism, their causes, symptoms and treatment options.
3) Diagnostic tests for thyroid disorders including thyroid function tests and scans.
4) Specific conditions like Graves' disease, Hashimoto's thyroiditis, thyroid storm and their characteristics.
This document discusses thyroid hormones, their functions, synthesis, regulation, and mechanisms of action. It covers the receptors, transporters, and enzymes involved in thyroid hormone activity. It also describes the clinical features and management of hypothyroidism and hyperthyroidism, as well as laboratory tests for thyroid function. Various thyroid analogs and their selective actions on thyroid hormone receptors are also mentioned.
This presentation about thyroid gland :
- Anatomy of thyroid gland
- Physiology of thyroid gland
- Pathology of thyroid gland
- Treatment and prevention of thyroid disease
The thyroid gland produces three main hormones: T4, T3, and calcitonin. T4 is produced in larger amounts than T3. Both are produced through a process involving iodine uptake and binding to tyrosine residues on thyroglobulin within the thyroid follicle. T3 has greater biological activity than T4. Hypothyroidism occurs when not enough hormones are produced, while hyperthyroidism is an overproduction. Diseases are treated through antithyroid drugs, radioactive iodine therapy, or thyroid surgery.
The thyroid gland regulates metabolism and plays a key role in many body functions. Hypothyroidism occurs when the thyroid gland is underactive and does not produce enough hormones. It can be caused by autoimmune diseases like Hashimoto's thyroiditis or problems with the pituitary gland. Symptoms include fatigue, weight gain, dry skin and hair, and feeling cold. Blood tests are used to diagnose hypothyroidism by measuring thyroid stimulating hormone and thyroid hormone levels. Lifelong thyroid hormone replacement therapy is needed to treat hypothyroidism and prevent serious complications like myxedema coma.
The thyroid gland secretes two major hormones: thyroxine (T4) and triiodothyronine (T3). These hormones increase the metabolic rate of the body and are controlled by thyroid-stimulating hormone (TSH) from the pituitary gland. The thyroid traps iodine from the blood and uses it to synthesize T4 and T3 within thyroglobulin follicles. Most secreted hormone is T4, which is later converted to the more potent T3 in tissues. Thyroid hormones increase metabolism, growth, and heart rate by activating nuclear transcription of genes in cells throughout the body. TSH secretion from the pituitary is regulated by thyrotropin-releasing hormone from the hyp
This document discusses thyrotoxicosis, which results from excess thyroid hormone production regardless of cause. It is one of the more common endocrine disorders seen by family physicians. The causes of thyrotoxicosis include Graves' disease, toxic multinodular goiter, solitary toxic nodule, and thyroiditis. Graves' disease is an autoimmune condition characterized by a diffuse goiter, ophthalmopathy, and dermopathy. Toxic multinodular goiter develops from autonomy in a pre-existing nodular goiter. A solitary toxic nodule refers to autonomy developing in an otherwise normal thyroid. Thyroiditis can cause a transient thyrotoxic phase followed by hypothyroidism. Treatment depends on
Thyroid Function Tests, NORMAL THYROID PHYSIOLOGY
, Anatomy of the Thyroid Gland, Hypothalamic-Pituitary-Thyroid AxisNegative Feedback Mechanism, Hypothalamic-Pituitary-Thyroid AxisPhysiology, PITUITARY-THYROTROPE CELL
, THYROID HORMONES
, FORMATION & SECRETION OF THYROID HORMONES , ION TRANSPORT BY THE THYROID FOLLICULAR CELL
, THYROGLOBULIN SYNTHESIS IN THE THYROID FOLLICULAR CELL
Thyroid and its pathology (Hypothyroidism).Vikas Reddy
GREEK :- THYREOS – SHIELD ; EIDOS – FORM
1.LOCATION:- Anterior to trachea in between the cricoid cartilage and the suprasternal notch.
2.SHAPE:- It has 2 lobes connected with an isthmus, each lobe in turn has two poles.
3.Weighs around 10-20 gm, highly vascular and soft in consistency.
4. 4 Parathyroid glands which secrete PTH are located posterior to each pole of thyroid
The RLN traverse the lateral border of thyroid gland and must be identified during thyroid surgery to avoid injury and vocal cord paralysis.
Develops from the floor of primitive pharynx during the 3rd week of gestation.
Fetal cells in which developmental transcription factors TTF-1,TTF-2 & PAX-8 are expressed selectively form the thyroid gland ,secondly they result in induction of thyroid specific genes
Tg,TPO,NIS,TSH-R.
Mutations-THYROID AGENESIS & DYSHORMONOGENESIS(CONG. HYPOTHYROIDISM).
The developing gland migrates along the thyroglossal duct to reach its final location in the neck.
LINGUAL THYROID AND THYROGLOSSAL DUCT CYST.
Thyroid hormone synthesis begins at about 11 weeks of gestation.
Until 11 week of gestation and even later, it is the maternal thyroid hormones which cross the placenta to reach the fetus and aid its development.
Therefore a child born to a hypothyroid mother would suffer from features of congenital hypothyroidism.
Secondly if the mother has TSH-R blocking antibodies or has received anti thyroid therapy during pregnancy, might lead to transient congenital hypothyroidism.
The thyroid gland secretes three main hormones: T4, T3, and calcitonin. T4 is secreted in larger amounts than T3 but T3 has higher biological activity. The thyroid takes up iodine from the bloodstream which is then oxidized and used to iodinate tyrosine residues on thyroglobulin in the follicles. Coupling of iodinated tyrosines produces T4 and T3 which are stored in the follicles bound to thyroglobulin. TSH stimulates release of T4 and T3 into the bloodstream where most is bound to proteins while a small amount is free and biologically active. T4 can be converted to the more active T3 in other tissues
Thyroid function tests (TFTs) are the most frequently ordered endocrine investigations in children and adolescents.
Abnormalities in TFTs can help in diagnosis of primary thyroid disorders (i.e. disorders in which the defect is at the thyroid level) as well as secondary or central thyroid disorders (in which defect is at the pituitary level).
The document discusses thyroid hormones and thyroid inhibitors. It describes:
1. The thyroid gland secretes three hormones - thyroxine (T4), triiodothyronine (T3), and calcitonin. T4 and T3 are produced in the thyroid follicles and influence metabolism, growth, and development.
2. Thyroid hormones are synthesized through iodide uptake, oxidation, iodination, coupling of amino acids, storage in thyroglobulin, and release. Peripheral tissues convert some T4 to the more active T3.
3. Thyroid disorders like hypothyroidism and hyperthyroidism can be treated with thyroid hormone replacement or inhibitors like antithy
The thyroid gland regulates metabolism by secreting thyroid hormones like thyroxine (T4) and triiodothyronine (T3). The thyroid takes up iodine from the bloodstream and uses it to produce T4 and T3 by binding iodine to tyrosine residues on thyroglobulin inside thyroid follicles. Thyroid-stimulating hormone (TSH) from the pituitary gland controls thyroid function and hormone production. Most thyroid hormones circulate bound to transport proteins like thyroxine-binding globulin (TBG) while a small fraction remains free and active. The thyroid and its hormones play a vital role in maintaining normal growth, development, and metabolism throughout the body.
This document summarizes the key aspects of thyroid hormone production and regulation. It describes how the thyroid gland produces the hormones thyroxine (T4) and triiodothyronine (T3) from iodine and the amino acid tyrosine. It also explains how thyroid hormone production and secretion is regulated through a negative feedback loop involving the hypothalamus, pituitary gland, and thyroid itself. Specifically, it details how thyroid stimulating hormone (TSH) from the pituitary stimulates the thyroid in response to thyrotropin-releasing hormone (TRH) from the hypothalamus, and how high thyroid hormone levels inhibit this process.
1. The thyroid gland secretes T3 and T4 hormones which regulate metabolism. Hypothyroidism is treated with levothyroxine replacement while hyperthyroidism is treated with antithyroid drugs like methimazole or propylthiouracil.
2. Methimazole and propylthiouracil work by inhibiting thyroid peroxidase and iodination of tyrosine, blocking thyroid hormone production. Propylthiouracil also blocks conversion of T4 to T3.
3. Treatment of hyperthyroidism in pregnancy uses propylthiouracil in the first trimester and methimazole in the second and third trimesters due to safety.
This slideshow gives you a information about hormone thyroid and its clinical activity and molecular mechanism. And also hormone abnormalities and drugs used to treat them .
hyperthyroidism and hypothyroidism is discussed along with drugs used to overcome those condition.
- The thyroid gland is the largest, butterfly-shaped endocrine glands & is located at the base of the neck immediately below the Larynx, on each side of & anterior to the trachea.The thyroid gland consists of two lobes of endocrine tissue (lying on either side of trachea) joined in the middle by a narrow portion of the gland called as the Isthmus.The thyroid has one ofthe highest rates of blood flow per gram of tissue. - In a normal adult male, it weighs 15-20 g but is capable of enormous growth, sometimes achieving a weight of several hundred grams.
The document provides an overview of the anatomy, physiology, and pathology of the thyroid gland. It discusses:
- The anatomy of the thyroid gland including its location in the neck and blood supply.
- Thyroid hormone synthesis which involves iodine uptake and incorporation into thyroglobulin to form T3 and T4.
- Regulation of the thyroid axis by TSH from the pituitary gland and thyroid hormone feedback.
- Types of thyroiditis including acute, subacute, silent, drug-induced, and chronic forms. Subacute thyroiditis is the most common type and can cause transient hypo- or hyperthyroidism.
- Treatment for thyroiditis depends on the type but may
The thyroid gland secretes the hormones thyroxine (T4) and triiodothyronine (T3), which regulate metabolism and growth. T4 makes up the majority of thyroid hormones produced, but T3 is the more biologically active form. Their secretion is controlled by TSH from the pituitary gland. Thyroid hormones increase basal metabolic rate, stimulate lipid, carbohydrate and protein metabolism, and affect growth and development, especially of the nervous system. They also increase heart rate and contractility, causing a hyperdynamic circulation.
The document discusses the structure and function of the thyroid gland. It describes the gland's lobes and isthmus, as well as the follicles that contain colloid and thyroid hormones like T3 and T4. The process of thyroid hormone production, secretion, and regulation by the hypothalamic-pituitary-thyroid axis is explained in detail. The actions of thyroid hormones on metabolism, growth, and various organ systems are also outlined.
Molecular and Cellular Mechanism of Action of Thyroid_Anas_Saifi.pptxashharnomani
This document provides an overview of the molecular and cellular mechanisms of thyroid hormone action. It discusses the chemistry, biosynthesis, transport, receptors, regulation of secretion, and mechanisms of action of the thyroid hormones T3 and T4. It also describes their various effects in the body as well as clinical applications such as replacement therapy and anti-thyroid drugs that interfere with thyroid hormone synthesis.
The document summarizes key aspects of the thyroid gland and its functions. It discusses that the thyroid gland secretes thyroid hormones that regulate metabolism and calcium levels. The primary hormones secreted are thyroxine (T4) and triiodothyronine (T3). Iodine is essential for thyroid hormone synthesis and is taken up by the thyroid and kidneys. Within the thyroid, iodine is added to thyroglobulin which is then degraded, releasing T4 and T3 into circulation. Thyroid stimulating hormone (TSH) regulates thyroid function by stimulating hormone synthesis and secretion.
Thyroid function tests help to determine if your thyroid is not working correctly. If blood levels of thyroid hormone are high, the brain senses this and sends a message to stop producing TSH.
The thyroid gland develops from endodermal thickening in the floor of the mouth and descends to its final location in the neck. It normally forms by week 7 and contains two lobes connected by an isthmus. Congenital abnormalities can include thyroglossal cysts or lingual thyroid. The thyroid produces T4 and T3 hormones which regulate metabolism. Hyperthyroidism includes Graves' disease, while hypothyroidism is often Hashimoto's thyroiditis. Treatment involves restoring normal thyroid levels through medication.
THYROID HORMONE.pptx by Subham Panja,Asst. Professor, Department of B.Sc MLT,...Subham Panja
The document summarizes the thyroid gland and its hormones. It discusses that the thyroid gland produces three hormones: thyroxine (T4), triiodothyronine (T3), and calcitonin. T4 makes up 90% of hormone production while T3 is 9-10%. The hormones are synthesized from iodine and tyrosine, stored in thyroglobulin vesicles, and released into blood circulation via binding proteins. The hormones act to increase basal metabolic rate and stimulate growth, accelerating protein synthesis and mitochondrial activity in most tissues.
This document summarizes the process of thyroid hormone synthesis and function. It describes how iodine is transported into thyroid cells and used to produce the hormones thyroxine (T4) and triiodothyronine (T3) through oxidation and coupling reactions incorporated into thyroglobulin. The hormones are stored and later released from thyroglobulin and transported bound to plasma proteins in the bloodstream. The majority of the released hormone is T4, which is converted to the active form T3 in tissues. The hormones increase metabolism by binding to nuclear receptors and altering gene expression. Disorders of the thyroid that cause over- or underactive function like Graves' disease, multinodular goiter, Hashim
The document summarizes the structure, location, and functions of the thyroid gland. It notes that the thyroid gland has a butterfly shape with two lobes connected by an isthmus. It regulates metabolism and other bodily functions through hormones like thyroxine and triiodothyronine. When overactive, it can cause hyperthyroidism and goiter; when underactive, it can cause hypothyroidism, cretinism, or myxedema. The parathyroid glands help regulate blood calcium levels through parathyroid hormone and calcitonin.
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This document provides an overview of hypothyroidism, including its definition, effects on different organ systems, types, causes, investigations, and treatment. Some key points are:
- Hypothyroidism is a deficiency in thyroid hormone secretion, occurring in 2-15% of the population more commonly in women. Risk increases with age.
- It affects the cardiovascular, respiratory, renal, central nervous, neuromuscular, gastrointestinal, and hematological systems, causing decreased metabolism.
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Thyroid gland (anatomy and physiology) biochemical basis
1. Clinical Scenario
• A 65-year-old female presents to the clinic feeling tired and
fatigued all the time.
• She has also noticed an increasing problem with constipation
despite adequate fiber intake. She is frequently cold when
others are hot.
• Her skin has become dry, and she has noticed a swelling
sensation in her neck area.
• On examination she is afebrile with a pulse of 60 beats per
minute.
• She is in no acute distress and appears in good health. She has
an enlarged, nontender thyroid noted on her neck.
• Her reflexes are diminished, and her skin is dry to the touch.
• Her daily dietary chart was normal but fortified salt is missing.
2. • What is the most likely diagnosis?
• What laboratory test would you need to confirm the
diagnosis?
• What is the treatment of choice?
4. Introduction:
• Named after the thyroid cartilage
• Greek: Shield shaped
• One of the largest endocrine glands
• Produces Thyroid hormones and
Calcitonin
• Plays role in metabolism, growth
and calcium homeostasis.
5. Uniqueness
• Easily seen and palpated
• Iodine
• Stored in an extracellular site
• Peptide hormones - no cell-membrane receptors
• Nuclear receptors.
7. Anatomy:
• Brownish-red gland.
• Butterfly shape gland ( H or U shaped).
• Located anteriorly in the lower neck
• Extending from the level of the fifth cervical
vertebra down to the first thoracic vertebra.
• Two lobes are present
• Lobes of gland are attached to each other by
Isthmus.
• In some people a third “pyramidal lobe” exists,
ascending from the isthmus towards hyoid bone
8. • Each lobe is 50-60 mm long
• Its weight averages 25-30 g.
• It is slightly heavier in women.
• The gland enlarges during menstruation and
pregnancy.
• Parathyroid glands usually lie between
posterior border of thyroid gland and its
sheath
• Usually 2 on each side of the thyroid.
9. Arterial Supply:
• Highly vascular
• Main supply from :
Superior thyroid arteries
Inferior thyroid arteries
Venous Drainage:
• Superior thyroid veins drain superior poles
• Middle thyroid veins drain lateral parts
• Inferior thyroid veins drain inferior poles
10. Lymphatic drainage:
Drain to:
• Prelaryngeal LN’s, Pretracheal and Paratracheal LN’s,
Cervical LN’s
• Some drainage directly into brachio-cephalic LN’s
Innervations:
• Principal innervation of the thyroid gland derives from
the autonomic nervous system.
• Parasympathetic fibers come from the vagus nerves.
• Sympathetic fibers are distributed from the superior,
middle, and inferior ganglia of the sympathetic
trunk.
12. • Thyroid gland contains numbers of spherical
structures i.e. Follicles.
• Follicles are the basic functional unit of this gland
• It consists of
1. Follicular cells
2. Colloids.
13. Follicular cells:
• Follicular cells are normally cuboidal in shape
• Contain many small apical vesicles
• It transports ions
• Synthesize thyroglobulin
Colloids:
• Viscous gel consisting mostly of iodinated thyroglobulin.
• Thyroid follicles are separated from each other by
connective tissue containing capillaries and another type
of cells Parafollicular cells or C cells. These cells release
Calcitonin.
15. Physiology:
Thyroid gland is responsible for:
• Homeostasis of all cells
• Cell differentiation, growth, and metabolism
These physiological functions are performed by
synthesizing two principal hormones
• Thyroxine (T4 ) and triiodothyronine (T3)
17. Source of Iodine:
• Available through certain foods (seafood, bread,
dairy products), iodized salt, or dietary supplements,
as a trace mineral
• The recommended minimum intake is 150 μg/day
18. Fate of iodine
• Dietary iodine (I) is main source
• Dietary iodine reaches the circulation as iodide ion, an anion.
• Iodide from plasma is actively transported by a sodium-iodine symporter.
• Then iodide oxidizes to form iodine.
• At the apical membrane of cell Pendrin protein and apical iodide
transporter (AIT) is present which mediates iodide efflux into colloid.
• Iodide accumulation in the thyroid is an active transport process that is
stimulated by thyroid stimulating hormone (TSH).
• In lacuna, iodide is oxidized (“organified”) to an iodine radical by the
thyroperoxidase (TPO) enzyme
• TPO catalyses the monoiodination, diiodination and coupling reaction
• In the follicular cells, the iodine concentration is 30- to 40-fold greater
than the circulating concentration.
• Iodide transport is inhibited by lithium, which competes with sodium.
• Antithyroid drugs such as propylthiouracil and methimazole inhibit
iodination and coupling
19.
20. Production of Thyroglobulin:
• The follicle cells of the thyroid produce thyroglobulin
• Thyroglobulin is a very large glycoprotein.
• Thyroglobulin is released into the colloid space
• Tg is a glycoprotein homodimer of 660 kDa.
• A total of 134 tyrosine residues are found in the
homodimer, and 25 to 30 of these residues are
iodinated.
• TSH is the principal stimulator of Tg synthesis.
• Thyroid transcription factor 1 (TTF1) interacts with the
Tg promoter to stimulate Tg mRNA synthesis
21.
22. Oxidation of Iodide and Iodination of
Thyroglobulin:
• Iodide must be oxidized to be able to iodinate tyrosyl
residues of Tg
• Iodination of the tyrosyl residues then forms
monoiodotyrosine (MIT) and diiodotyrosine (DIT), which
are then coupled to form either T3 or T4
• Both reactions are catalysed by Thyroid Peroxidase(TPO).
23. Thyroperoxidase (TPO):
• TPO catalyzes the oxidation steps involved in Iodide activation,
iodination of Tg tyrosyl residues, and coupling of iodotyrosyl
residues
• TPO has binding sites for Iodide and tyrosine
• TPO uses H2O2 as the oxidant to activate Iodide to hypoiodate (OI-),
the iodinating species
24. Proteolysis of Tg With Release of
thyroid hormones:
• T4 and T3 are synthesized and stored within the Tg
molecule
• Proteolysis is an essential step for releasing the
hormones
• To liberate T4 and T3, Tg is resorbed into the
follicular cells in the form of colloid droplets,
Pinocytosis.
• Which then fuse with lysosomes to form
phagolysosomes
• Tg is then hydrolyzed to T4 and T3, which are then
secreted into the circulation
25. Wolff-Chaikoff Effect:
• It is an auto regulatory phenomenon that inhibits
organification in the thyroid gland.
• This becomes evident secondary to elevated levels of
circulating iodide.
• It lasts several days (around 10 days),
• After which it is followed by an ‘escape phenomenon’
which is resumption of normal organification of iodine
• Escape phenomenon is believed to occur because of
decreased inorganic iodine concentration secondary to
down-regulation of sodium-iodide symporter.
26. Jod-Basedow Effect:
• Opposite of the Wolff-Chaikoff effect
• Excessive iodine loads induce hyperthyroidism
• Observed in hyperthyroid disease processes
– Graves’ disease
– Toxic multinodular goiter
– Toxic adenoma
• This effect may lead to symptomatic thyrotoxicosis in
patients who receive large iodine doses from
– Dietary changes
– Contrast administration
– Iodine containing medication ( Amiodarone )
27. Hormonal Transport:
• More than 99% of circulating T4 and T3 is bound to
plasma carrier proteins
• Thyroxine-binding globulin (TBG), binds about 75%
• Transthyretin (TTR), also called thyroxine-binding
prealbumin (TBPA), binds about 10%-15%
• Albumin binds about 7%
• High-density lipoproteins (HDL), binds about 3%
• Carrier proteins can be affected by physiologic
changes, drugs, and disease
28. Free Hormone Concept:
• Only unbound (free) hormone has metabolic activity
and physiologic effects
• Free hormone is a tiny percentage of total hormone in
plasma (about 0.03% T4; 0.3% T3)
• Although the total molar concentration of T4 is 50 times
that of T3, the concentration of free T4 is only about 3
times that of free T3.
• Only free fraction of thyroid hormone is able to cross
the plasma membrane and enter the nucleus.
29. Conversion of T4 to T3:
• T4 is the primary secretory product of the thyroid gland, which is
the only source of T4
• The thyroid secretes approximately 70-90 μg of T4 per day
• T3 is derived from 2 processes
• The total daily production rate of T3 is about 15-30 μg
• About 80% of circulating T3 comes from deiodination of T4 in
peripheral tissues
• About 20% comes from direct thyroid secretion
• Sites of T4 Conversion:
• The liver is the major extrathyroidal site for production of T3
• Some T4 to T3 conversion also occurs in the kidney.
• This conversion is possible in the presence of iodothyronine
deiodinases (D1, D2 and D3).
• D1 and D2 helps in forming T3 from T4.
• D1 and D3 helps to form inactive form rT3.
31. Mechanism of Action of T3:
• T3 enters plasma membrane then to nucleus
• Specific transporters facilitate the entry into cell.
• The organic anion transporting polypeptides (OATPs) and
human monocarboxylate transporter 8 (MCT8) are active
transporters
• OATPs are specific for T4 and rT3 whereas MCT8 for T3
• In nucleus it interacts with thyroid hormone receptor (THR)
• Several alpha and beta isoforms of THR are produced.
• THR usually dimerize with the retinoid X receptors(RXRs)
• The formation of the T3-THR/DNA (thyroid hormone receptor
element) complex with recruitment of transcriptional coactivators
leads to activation of target genes
• Giving rise to mRNA and protein production.
33. • 4 intranuclear T3 receptors: α1, α2, β1 and β 2;
• nonfunctional receptor: α2.
• The different forms of thyroid receptors have patterns
of expression that vary by tissue and by developmental
stage.
• The presence of multiple forms of the thyroid hormone
receptor, with tissue and stage-dependent differences in
their expression, suggests an extraordinary level of
complexity in the physiologic effects of thyroid
hormone.
34.
35. Thyroid hormone actions:
1. Growth and development:
• Stimulates formation of proteins, which exert trophic
effects on tissues
• Increase growth and maturation of bone
• Increase tooth development and eruption
• Increase growth and maturation of epidermis, hair
follicles and nails
36. 2. Nervous System:
• Critical for normal CNS neuronal development
• Enhances wakefulness and alertness
• Enhances memory and learning capacity
• Required for normal emotional tone
• Increase speed and amplitude of peripheral nerve
reflexes
39. 6. Reproductive System:
• Required for normal follicular development and ovulation
in the female
• Required for the normal maintenance of pregnancy
• Required for normal spermatogenesis in the male
40. 7. Basal metabolic rate:
• T3 increases basal metabolic rate
• Activity of the Na+/K+ pump uses up energy, in the form of
ATP
• About 1/3rd of all ATP in the body is used by the Na+/K+
ATPase
• T3 increases the synthesis of Na+/K+ pumps, markedly
increasing ATP consumption.
8. Calorigenic effects:
• T3 increases oxygen consumption by most peripheral
tissues
• Increases body heat production
41. 9. Metabolic effect:
• Stimulates lipolysis and release of free fatty acids and
glycerol
• May leads to fall in plasma cholesterol
• Increase glucose absorption.
• Increase gluconeogenesis and glycogenolysis.
• Increase insulin breakdown.
42. Hypothalamic-Pituitary-Thyroid Axis:
• Other hormones play role in synthesis of thyroid
hormones.
• Thyroid Stimulating Hormone (TSH) helps in synthesis of
thyroid hormones.
• TSH is tropin hormone.
• Synthesis of TSH is itself controlled by other hormone
• Thyrotropin Releasing Hormone (TRH) is responsible for
production of TSH.
43.
44. Thyrotopin Releasing Hormone:
• A tripeptide: pyroGlutamate-histidine-proline-amide
• Synthesized from a 29 kDa precursor protein
• Produced by Hypothalamus, medial neurons of the
paraventricular nucleus.
45. • Thyrotropin-releasing hormone is very short-lived, lasting
for a matter of two minutes.
• Travels less than an inch in the bloodstream to the pituitary
gland before it is broken down.
• Release is pulsatile, circadian
• Travels through portal venous system to
adenohypophysis
• Stimulates TSH formation
• Also stimulate the release of another hormone from the
pituitary gland, prolactin.
46. Influence of TRH on TSH Release:
• TRH is a hypothalamic releasing factor which travels through
the pituitary portal system to act on anterior pituitary
thyrotroph cells.
• TRH acts through G protein-coupled receptors, activating the
IP3 (Ca2+) and DAG (PKC) pathways to cause increased
production and release of TSH.
TRH phospholipase C
G protein-coupled
receptor
IP3 calcium
DAG PKC
calmodulin
47. Thyroid Stimulating Hormone:
• It is a glycoprotein hormone synthesized and secreted by
thyrotrope cells in the anterior pituitary gland.
• Its secretion follows circardian rhythm, highest between
midnight and 4 AM and lowest at midday
• Consists of two subunits, the
alpha and the beta subunit.
48. • The α (alpha) subunit is nearly identical to that of human
chorionic gonadotropin (hCG), luteinizing hormone
(LH), and follicle-stimulating hormone(FSH).
• The α subunit is thought to be the effector region
responsible for stimulation of adenylate cyclase (involved
the generation of cAMP)
• The β (beta) subunit (TSHB) is unique to TSH, and
therefore determines its receptor specificity
• The α chain has a 92-amino acid sequence.
• The β chain has a 118-amino acid sequence.
49. • Thyroid hormones exert negative feedback on TSH
release by:
• inhibition/stimulation of TSH synthesis
• decreasing/increasing pituitary receptors for TRH
50. Action of TSH on the Thyroid:
• TSH acts on follicular cells of the thyroid.
- increases iodide transport into follicular cells
- increases production and iodination of thyroglobulin
- increases endocytosis of colloid from lumen into follicular cells
Na+
I-
thyroglobulinfollicle
cell
gene
I-
endocytosis
thyroglobulin
T3 T4
colloid droplet
I-I+
iodination
thyroglobulin
Na+ K+
ATP
51. Mechanism of Action of TSH:
• TSH binds to a plasma membrane-bound, G protein-coupled
receptor on thyroid follicle cells.
• Specifically, it activates a G-coupled receptor, resulting in
increased cAMP production and PKA activation.
TSH
Gsa
Adenylyl
Cyclase
ATP cyclic AMP
Protein kinase
A
Follicle cell
52. Regulation of Thyroid Hormone
Levels:
• Thyroid hormone synthesis and secretion is
regulated by two main mechanisms:
• an “autoregulation” mechanism, which reflects the
available levels of iodine
• regulation by the hypothalamus and anterior pituitary
53. Autoregulation of Thyroid
Hormone Production:
• The rate of iodine uptake and incorporation into
thyroglobulin is influenced by the amount of iodide
available:
• low iodide levels increase iodine transport into follicular
cells
• high iodide levels decrease iodine transport into
follicular cells
• Thus, there is negative feedback regulation of
iodide transport by iodide.
54. Feedback mechanism:
• Increase and decrease in the thyroid hormone level can
itself maintain its level.
• When there is increase in Thyroid hormone level in
blood it inactivates TRH and TSH synthesis
• As a result there will be decrease production of thyroid
hormones
• And vice-versa.
• Thyroid hormones exert negative feedback on TSH
release at the level of the anterior pituitary.
55. Factors affecting Thyroid hormones:
Age:
Fetal Life:
• T4 and TSH are detectable at 10-12 weeks of gestation.
• At about 36 weeks total and free T4 reach adult level.
• However total and free T3 reach lower limit of adult range.
Neonate:
• There is rapid, transient release of TSH, T4 and T3 occurs.
• TSH levels peaks at first 30 mins, stimulates T3 and T4 production.
• This effect attenuated in premature birth.
56. Infancy and childhood:
• TSH and free T4 level are as adult range.
• Free T3 is higher than in adults.
Elderly:
• Modest decrease in T4
• Slight fall in T3 and TSH.
Pregnancy:
• There is rise in free T3 and T4 concentration due to thyroid
stimulating action of hCG.
• This lead to suppression of TSH.
• As pregnancy progress free hormone level decreases and TSH level
rise.
57. Drugs:
Mechanism Example of Drugs
Decrease in TSH secretion Dopamine, glucocorticoids, cytokines
Decrease in thyroid hormone secretion Lithium, amiodarone, iodine
Increase in thyroid hormone secretion iodine
Displacement of thyroid hormone from
plasma proteins
Furosemide, salicylates, NSAIDS
Increase hepatic metabolism Phenytoin, rifampicin, barbiturates
Impaired T4 and T3 conversion Beta antagonist, radiocontrast dye
Impaired absorption of thyroxine Calcium, sucralfate, soya protein
Modified thyroid hormone action amiodarone
58. Other factors:
• Thyroid hormone metabolism is markedly affected by fasting and
illness.
• There is release of dopamine, cortisol, somatostatin along with
cytokines which suppress TSH.
• Decrease production of T3, changes in function of T3 receptors leads
to low T3.
• Catecholamines and leptin stimulate TRH production hence regulate
TSH
59. Discussion to case
• Diagnosis: Iodine deficiency hypothyroidism (Goiter)
Iodine deficiency
Decrease synthesis of thyroid hormone
Decrease release of thyroid hormone
Stimulate pituitary to produce THS
Increase release of TSH
Increase cellularity of thyroid gland
Hyperplasia of thyroid
Goiter
Visible neck mass
Weezing and coughing
Fatigue
Dyspagia
Weight gain
pain
60. • Laboratory tests: TSH and free T4
• Treatment: Iodine supplementation on diet and
Thyroid hormone replacement with levothyroxine
Diagnosis: Hypothyroidism
Laboratory tests: TSH and free T4
Treatment: Thyroid hormone replacement with levothyroxine
like most peptide hormones, T4 and T3 are made as part of a larger protein
only endocrine gland easily seen and palpated
require an essential trace element, iodine, for the production of active hormone
hormone is stored in an extracellular site within a highly proteinaceous material called thyroid colloid
unlike peptide hormones, there are no cell-membrane receptors for these hormones.
Instead, like the steroid hormones, thyroid hormones act by binding to nuclear receptors and regulate the transcription of cell proteins.
Perchlorate is use to block uptake of iodine/ thiocyanates competitively inhibit the iodine pump but not taken up by gland.
Although most Tg is secreted into the follicular lumen, a
small amount of Tg is released from the follicular cells without
transport into the colloid, and this Tg is not iodinated. Of
consequence in autoimmune thyroid disease, iodination
increases the immunogenicity of Tg.
Dual oxidases duox also plays role
Mit and dit are stripped of by dehalogenase (dhal).
Large excess of iodide given acutely inhibits the adenylate cyclase response to TSH.
Not seen in normal individual
T4 is more tightly bound to thanT3
T4 is prohormone T3 is responsible for the biological actions.
organic anion transporting polypeptides (OATPs)
human monocarboxylate transporter 8 (MCT8)